Endothelin (ET), a potent endogenous vasoconstrictor, is produced by the endothelin. High amounts of ET are found in the urine compared to low levels in plasma. Although much has been learned about the structure and biological effects of ET, little is known about the regulation of the urinary excretion of ET (UETV). We investigated 1) The effects of angiotensin II (A-II), arginine vasopressin (AVP) and nifedipine on UETV. 2) The effects of the non specific A-II antagonist - Saralasin and the specific A-II non peptide antagonist - losartan on the stimulatory effect of A-II on UETV. 3) The effect of converting enzyme inhibition by captopril on the stimulatory effect of nifedipine on the UETV. A-II (50 and 500 ng/kg/min) caused significant increases in urine flow (V), mean arterial pressure (MAP) and 10-30 fold increases in UETV. Pretreatment of the rats with saralasin (1-3 mg) significantly reduced V and MAP but not UETV. Infusion of saralasin alone caused a significant increase in UETV without affecting the MAP or V. Pretreatment of the rats with losartan (10 mg/kg) totally blocked the increases in MAP and UETV induced by A-II. AVP (10 and 100 increases/kg/h) administration induced similar hypertensive and diuretic responses as A-II, but did not alter UETV. Infusion of nifedipine (0.1 and 1.0 mg/kg/h) increased UETV 3-10 fold. Pretreatment of the rats with converting enzyme inhibitor (captopril- 1mg/kg/h) abolished that increase.